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Larry Moran: Vitamin C Pseudogene is Powerful Evidence

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In his on-going criticism of Jonathan Wells’ new book, The Myth of Junk DNA, evolutionist Larry Moran now asserts that the much discussed vitamin C pseudogene is powerful evidence for evolution and common descent:  Read more

Comments
Elizabeth, you simply do not have the evidence to back your assertion for 'vertical evolution'. Sub-speciation in fact explains the evidence much better than evolution since information is lost in the sub-speciation events, as well it agrees with the overall pattern we find in the fossil record; i.e. abrupt appearance and Disparity of major lifeforms precedes diversity of sub-species within the novel major lifeforms: The unscientific hegemony of uniformitarianism - David Tyler - May 2011 Excerpt: Evolution has been implicitly viewed as a uniformitarian process where the rates may vary but the underlying processes, including the types of variation, are essentially invariant through time. Recent studies demonstrate that this uniformitarian assumption is false, suggesting that the types of variation may vary through time. http://www.arn.org/blogs/index.php/literature/2011/05/16/the_unscientific_hegemony_of_uniformitar Here is a page of quotes by leading paleontologists on the true state of the fossil record: https://docs.google.com/document/pub?id=15dxL40Ff6kI2o6hs8SAbfNiGj1hEOE1QHhf1hQmT2Yg ================ Elizabeth, for you to stay scientific, you must demonstrate a method that can generate functional information over and above what was already in the parent species, that does not include intelligence. By the way Elizabeth, there is a million dollar prize for demonstrating a purely material process that is capable of producing functional information: "The Origin-of-Life Prize" ® (hereafter called "the Prize") will be awarded for proposing a highly plausible natural-process mechanism for the spontaneous rise of genetic instructions in nature sufficient to give rise to life. The explanation must be consistent with empirical biochemical, kinetic, and thermodynamic concepts as further delineated herein, and be published in a well-respected, peer-reviewed science journal(s). http://lifeorigin.info/ The Law of Physicodynamic Insufficiency - Dr David L. Abel - November 2010 Excerpt: “If decision-node programming selections are made randomly or by law rather than with purposeful intent, no non-trivial (sophisticated) function will spontaneously arise.”,,, After ten years of continual republication of the null hypothesis with appeals for falsification, no falsification has been provided. The time has come to extend this null hypothesis into a formal scientific prediction: “No non trivial algorithmic/computational utility will ever arise from chance and/or necessity alone.” http://www.scitopics.com/The_Law_of_Physicodynamic_Insufficiency.htmlbornagain77
May 28, 2011
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So the Vitamin C pseudogene is powerful evidence for evolution and common descent, until it isn't. What a wonderful theory. So accommodating.Mung
May 28, 2011
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Well, bornagain77, I should make my position clear: I don't "believe in Design", in the sense that you probably mean it. I agree with IDists that certain phenomena have a signature "complexity" that indicates something special about their origins, but I don't think that special something is what is normally meant by "intelligence". So I'm not an IDist. But unlike some, perhaps, I think that intelligence and design are perfectly amenable to scientific investigation, not surprisingly as I am a cognitive neuroscientist interested in the neural substrates of decision-making! Regarding the Y chromosome argument - I'm not entirely sure what you are saying - are you saying that because chimp Y chromosomes are very different from human Y chromosomes that they can't have a shared ancestor? Why? Obviously there are genetic differences between chimps and humans - why shouldn't these inclued the (very small number of) genes on the Y chromosome? Regarding speciation: ALL speciation is from a "parent lineage". That's what speciation is. And shortly after the speciation process (i.e. when what was a single population has diverged into two non-interbreeding populations) the two daughter populations will be very similar, and one may be more similar to the parent population than the other. And, as you agree, that has been observed. But that is ALL that is postulated by standard biological models of speciation, there isn't another "type of speciation that neo-Darwinists need to make their case" - what alternate "type of speciation" did you have in mind? The speciation of populations into separate non-interbreeding populations that occupy different ecological niches is exactly what standard models of evolution propose. In addition (and perhaps this is what you were referring to), a single population may evolve adaptively over time, without speciating (i.e. without diverging into two populations) by means of changing selection pressures acting on variation, but again, this has been observed in both the field and the lab (what is sometimes called "microevolution". Sure, over the short term, this will tend to be cyclical (as with the Galapagos finches you refer to), but high frequency oscillations do not preclude low-frequency drift, which indeed is what you would predict - if, for example, climate change in the future increases the frequency of el Nino events in the Galapagos, then you'd expect finch beak sizes to cease oscillating and instead drift to a new mean. Wouldn't you?Elizabeth Liddle
May 28, 2011
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Well Elizabeth, You are correct on Behe and if you believe in Design great, but as more evidence accumulates the common ancestry argument is nowhere near as stong as it once was. In fact, as was pointed out, using the very same line of reasoning on Y chromosome, produces a completely different conclusion. Thus you cannot make the argument consistently, which is a very 'suspect' thing as to rigorous methodology you are applying!!! As to this statement of yours;
'in other words it is strong evidence for the process of speciation. Which, indeed, has been actually observed.'
I'm sorry Elizabeth, that is simply not true, unless you mean SUB-speciation from a parent lineage, which is not the type of speciation that neo-Darwinists need to make their case! At one of her many public talks, she [Lynn Margulis] asks the molecular biologists in the audience to name a single unambiguous example of the formation of a new species by the accumulation of mutations. Her challenge goes unmet. Michael Behe - Darwin's Black Box - Page 26 Natural Selection and Evolution's Smoking Gun, - American Scientist - 1997 “A matter of unfinished business for biologists is the identification of evolution's smoking gun,”... “the smoking gun of evolution is speciation, not local adaptation and differentiation of populations.” Keith Stewart Thomson - evolutionary biologist “The central question of the Chicago conference was whether the mechanisms underlying microevolution can be extrapolated to explain the phenomena of macroevolution. At the risk of doing violence to the position of some people at the meeting, the answer can be given as a clear, No.” Roger Lewin - Historic Chicago 'Macroevolution' conference of 1980 Evolution - Tested And Falsified - Don Patton - video http://www.metacafe.com/watch/4036803 All examples of speciation put forth by materialists all turn out to be trivial examples of reproductive isolation: "The closest science has come to observing and recording actual speciation in animals is the work of Theodosius Dobzhansky in Drosophilia paulistorium fruit flies. But even here, only reproductive isolation, not a new species, appeared." from page 32 "Acquiring Genomes" Lynn Margulis. Selection and Speciation: Why Darwinism Is False - Jonathan Wells: Excerpt: there are observed instances of secondary speciation — which is not what Darwinism needs — but no observed instances of primary speciation, not even in bacteria. British bacteriologist Alan H. Linton looked for confirmed reports of primary speciation and concluded in 2001: “None exists in the literature claiming that one species has been shown to evolve into another.” http://www.evolutionnews.org/2009/05/selection_and_speciation_why_d.html Wired Science: One Long Bluff - Refuting a recent finch speciation claim - Jonathan Wells - Nov. 2009 Excerpt: "Does the report in Wired Science mean that “biologists have witnessed that elusive moment when a single species (of Galapagos finch) splits in two?” Absolutely not." http://www.evolutionnews.org/2009/11/wired_science_one_long_bluff.html This following study is very interesting for the researcher surveyed 130 DNA-based evolutionary trees to see if the results matched what 'natural selection' predicted for speciation and found: Accidental origins: Where species come from - March 2010 Excerpt: If speciation results from natural selection via many small changes, you would expect the branch lengths to fit a bell-shaped curve.,,, Instead, Pagel's team found that in 78 per cent of the trees, the best fit for the branch length distribution was another familiar curve, known as the exponential distribution. Like the bell curve, the exponential has a straightforward explanation - but it is a disquieting one for evolutionary biologists. The exponential is the pattern you get when you are waiting for some single, infrequent event to happen.,,,To Pagel, the implications for speciation are clear: "It isn't the accumulation of events that causes a speciation, it's single, rare events falling out of the sky, so to speak." http://www.newscientist.com/article/mg20527511.400-accidental-origins-where-species-come-from.html?page=2 As well, materialists never mention the fact that the variations found in nature (such as peppered moth color and finch beak size) which are often touted as solid proof of evolution are always found to be cyclical in nature. i.e. The variations are found to vary around a median position with never a continual deviation from the norm. This blatant distortion/omission of evidence led Phillip Johnson to comment in the Wall Street Journal: "When our leading scientists have to resort to the sort of distortion that would land a stock promoter in jail, you know they are in trouble."bornagain77
May 28, 2011
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Hi, bornagain77. Thankyou for your long and informative post. Well, as I said, I wasn't making a anti-design case from the broken GULO story, I was making a shared-ancestry case. I had understood that at least a substantial proportion of the ID community accepted common ancestry of at least fairly large subsets of modern populations, and I'd submit that the fact that the broken GULO gene is found in a primate clade (haplorrhini) defined by independent data is powerful evidence that haplorrhini primates share a common ancestor, even if that common ancestor was Intelligently designed and set down on earth a comparatively short (in conventional geological terms) time ago. Yes, indeed, the guinea pig also has a broken GULO gene, but as guinea pigs cannot be accommodated in the haplorrhini clade (they are not even primates), we must postulate a different ancestral breakage event for the guinea-pig version. Ditto for breakage in various species of passerines and also bats. The interesting thing is the distribution of these pseudogenes which tend to affect complete clades (as derived from independent data). This kind of evidence is the evidence that leads us to infer family tree for living things that includes, at its twigs, different species, in other words it is strong evidence for the process of speciation. Which, indeed, has been actually observed. That seems to me to be extremely well-established, but of course on its own is not an argument for Darwinian evolution, merely for common ancestry and speciation events, which presumably could also be accounted for in ID terms. So we are going to have to agree to differ on the issue of common ancestry! But as I understand it, common ancestry, per se, is no threat to ID, and I believe a number of ID proponents (including Behe, I think) embrace it.Elizabeth Liddle
May 28, 2011
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Good point Smidlee, Elizabeth, if, in your line of reasoning, small 'cherry picked' sequences nail the case shut for you for common descent, why in the world does not the entire Y chromosome, using your very same lime of reasoning, completely blow a hole in your common descent reasoning??? ========== Recent Genetic Research Shows Chimps More Distant From Humans,,, - Jan. 2010 Excerpt: A Nature paper from January, 2010 titled, "Chimpanzee and human Y chromosomes are remarkably divergent in structure and gene content," found that Y chromosomes in humans and chimps "differ radically in sequence structure and gene content," showing "extraordinary divergence" where "wholesale renovation is the paramount theme.",,, “Even more striking than the gene loss is the rearrangement of large portions of the chromosome. More than 30% of the chimp Y chromosome lacks an alignable counterpart on the human Y chromosome, and vice versa,,," http://www.evolutionnews.org/2010/04/recent_genetic_research_shows.html A False Trichotomy Excerpt: The common chimp (Pan troglodytes) and human Y chromosomes are “horrendously different from each other”, says David Page,,, “It looks like there’s been a dramatic renovation or reinvention of the Y chromosome in the chimpanzee and human lineages.” https://uncommondescent.com/intelligent-design/a-false-trichotomy/ Chimp and human Y chromosomes evolving faster than expected - Jan. 2010 Excerpt: "The results overturned the expectation that the chimp and human Y chromosomes would be highly similar. Instead, they differ remarkably in their structure and gene content.,,, The chimp Y, for example, has lost one third to one half of the human Y chromosome genes. http://www.physorg.com/news182605704.html The evolutionary scientists of the preceding paper offered some evolutionary 'just so' stories of 'dramatically sped up evolution' for why there are such significant differences in the Y chromosomes of chimps and humans, yet when the Y chromosome is looked at for its rate of change we find there is hardly any evidence for any change at all, much less the massive changes the evolutionists are required to explain. CHROMOSOME STUDY STUNS EVOLUTIONISTS Excerpt: To their great surprise, Dorit and his associates found no nucleotide differences at all in the non-recombinant part of the Y chromosomes of the 38 men. This non-variation suggests no evolution has occurred in male ancestry. http://www.reasons.org/interpreting-genesis/adam-and-eve/chromosome-study-stuns-evolutionistsbornagain77
May 28, 2011
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Elizabeth, you can't explain the origination of the GULO gene in the first place, nor can you even explain the origination of one protein by purely materialistic, neo-Darwinian, processes, which makes any conjecture you make as to common descent completely pointless as to you having a rigorous scientific foundation in which to make such claims!! But just to suppose you had any leg to stand on, scientifically, so as to make this conjecture, let's see how strong your evidence actually is compared to how strong you merely 'think' it is: Pseudogenes and the Origin of Humanity: A Response to the Venema Critique of the RTB Human Origins Model, Part 7 - Vitamin C refutation Excerpt: Yet, as biologist Peter Borger points out, fifty percent of the mutations in the primate and guinea pig exon X sequence are identical. In addition, the guinea pig exon X region shows a mutation at position 97, the location in the primate genomes where a deletion took place. These shared features could not have resulted because guinea pigs and primates shared a common ancestor. Instead, they must reflect nonrandom, reproducible changes. http://www.reasons.org/pseudogenes-and-origin-humanity-response-venema-critique-rtb-human-origins-model-part-7 Daniel Fairbanks Cherry Picks Data On Pseudogenes To Prop Up Common Descent - March 2011 Excerpt: What is particularly astonishing about Fairbanks’ citation is that the paper also documents the presence of shared deletions and substitutions in the GULO (Vitamin C) pseudogene of both humans and guinea pigs! Given that humans and guinea pigs are thought to have diverged at the time of the common ancestor with rodents, if the mutations are truly random, a mutational difference between the rat and guinea pig should not be shared by humans. But many mutational differences were shared by humans. Inai et al. argued that this was indicative of mutation hotspots where certain types of mutations occur with a greater frequency. The paper calculates the likelihood of these same substitutions in both humans and guinea pigs to be 1.87 x 10^-12. https://uncommondescent.com/intelligent-design/daniel-fairbanks-cherry-picks-data-on-pseudogenes-to-prop-up-common-descent/ Thus Elizabeth, we find upon a little closer inspection this 'cherry picked' sequence does not provide rigor as to support your claim. Even if you had the right to make the claim towards common ancestry in the first place!!! Further notes: Primate Phylogenetics Challenge Darwin's Tree of Life - Casey Luskin - Excellent Summary Level Audio Podcast http://intelligentdesign.podomatic.com/player/web/2011-05-09T16_32_00-07_00 Why Darwin was wrong about the (genetic) tree of life: - 21 January 2009 Excerpt: Syvanen recently compared 2000 genes that are common to humans, frogs, sea squirts, sea urchins, fruit flies and nematodes. In theory, he should have been able to use the gene sequences to construct an evolutionary tree showing the relationships between the six animals. He failed. The problem was that different genes told contradictory evolutionary stories. This was especially true of sea-squirt genes. Conventionally, sea squirts - also known as tunicates - are lumped together with frogs, humans and other vertebrates in the phylum Chordata, but the genes were sending mixed signals. Some genes did indeed cluster within the chordates, but others indicated that tunicates should be placed with sea urchins, which aren't chordates. "Roughly 50 per cent of its genes have one evolutionary history and 50 per cent another," Syvanen says. . "We've just annihilated the tree of life. It's not a tree any more, it's a different topology entirely," says Syvanen. "What would Darwin have made of that?" http://www.newscientist.com/article/mg20126921.600-why-darwin-was-wrong-about-the-tree-of-life.html Genetic Discoveries Uproot Darwin's Tree Of Life https://docs.google.com/document/d/1S5wXsukzkauD5YQLkQYuIMGL25I4fJrOUzJhONvBXe4/edit?hl=en_US# Widespread ORFan Genes Challenge Common Descent – Paul Nelson – video with references http://www.vimeo.com/17135166 Could Chance Arrange the Code for (Just) One Gene? "our minds cannot grasp such an extremely small probability as that involved in the accidental arranging of even one gene (10^-236)." http://www.creationsafaris.com/epoi_c10.htm "Estimating the Prevalence of Protein Sequences Adopting Functional Enzyme Folds” 2004: - Doug Axe ,,,this implies the overall prevalence of sequences performing a specific function by any domain-sized fold may be as low as 1 in 10^77, adding to the body of evidence that functional folds require highly extraordinary sequences." http://www.mendeley.com/research/estimating-the-prevalence-of-protein-sequences-adopting-functional-enzyme-folds/ ================= Embryonic development is now found to be unique for each mammalian species as well i.e. Chimps and humans have unique developmental pathways during embryogenesis!!!: The mouse is not enough - February 2011 Excerpt: Richard Behringer, who studies mammalian embryogenesis at the MD Anderson Cancer Center in Texas said, “There is no ‘correct’ system. Each species is unique and uses its own tailored mechanisms to achieve development. By only studying one species (eg, the mouse), naive scientists believe that it represents all mammals.” http://www.the-scientist.com/news/display/57986/ As well Elizabeth, the fossil record does not support you! Evolution of the Genus Homo - Annual Review of Earth and Planetary Sciences - Tattersall, Schwartz, May 2009 Excerpt: "Definition of the genus Homo is almost as fraught as the definition of Homo sapiens. We look at the evidence for “early Homo,” finding little morphological basis for extending our genus to any of the 2.5–1.6-myr-old fossil forms assigned to “early Homo” or Homo habilis/rudolfensis." “Dr. Leakey produced a biased reconstruction (of 1470/ Homo Rudolfensis) based on erroneous preconceived expectations of early human appearance that violated principles of craniofacial development,” Dr. Timothy Bromage Man is indeed as unique, as different from all other animals, as had been traditionally claimed by theologians and philosophers. Evolutionist Ernst Mayr When we consider the remote past, before the origin of the actual species Homo sapiens, we are faced with a fragmentary and disconnected fossil record. Despite the excited and optimistic claims that have been made by some paleontologists, no fossil hominid species can be established as our direct ancestor. Richard Lewontin - Harvard Zoologist “Something extraordinary, if totally fortuitous, happened with the birth of our species….Homo sapiens is as distinctive an entity as exists on the face of the Earth, and should be dignified as such instead of being adulterated with every reasonably large-brained hominid fossil that happened to come along.” Anthropologist Ian Tattersall (curator at the American Museum of Natural History)bornagain77
May 28, 2011
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@ post 16 I would think that not only you could trace the individual ancestor from the broken GULO gene but also by the man's Y chromosome. If the tribe had broken GULO gene but very different Y chromosomes (like man vs chimps) then I would think this would put serious doubts the broken gene came from the same man.Smidlee
May 28, 2011
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FMU Hunter point is they want to accept incredible odds when it's in their favor yet dismiss them when it's not. If the odds of two species have some of the same "deactivating mutations" of the Vitamin C gene separately are bad then how bad are the odds of creating this gene the start with?Smidlee
May 28, 2011
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That is your opinion. However you cannot support that with genetic data linking to the transformations required.
Well, we can have a decent shot at constructing a phylogeny from genetic data. But I can't support it personally, because it's not my field.
Do you really expect a broken gene to stay intact enough over thousands and thousands of generations all the while form-altering mutations are taking place?
No, like you, I'd expect a lot of mutations, and I'd predict, specifically, that the closer we think other haplorrhini primates are related to us (chimps and bonobos being closer than squirrel monkeys) the more similar their GULO genes to ours would be, and vice versa. That's one of the things that makes pseudogenes so useful in genetics - they accumulate mutations that aren't eliminated by selection. So I'd expect that a phylogeny based on DNA similarities in the GULO gene in happlorhini primates to map closely on to phylogenies constructed from other data. Indeed, that's a direct testable prediction arising from your premise, as I'm sure you agree. And as far as I know, it's supported by evidence. I'll try to look up the research later, gotta go to the post office right now! Cheers LizzieElizabeth Liddle
May 28, 2011
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OK, thanks:
Not required. 1- Perhaps it was never a useful gene in all organisms- meaning it could have some other function 2- It was useful but then became disabled in several populations- mutational hot spots exist and a mutation via a common mechanism similarly disabled the working genes. Only populations that could supplement their diet (epigenetics) survived.
Well, those are testable hypotheses, so,cool. But common ancestry of haplorrhini is also a very viable hypothesis, and supported by a large amount of evidence. But sure, it's always good to look at alternative theories, which is why:
...we can make up any story we want to as long as it supports our cause
and as long as we then develop it into a testable hypothesis that we then test. Oh, and it doesn't have to support "our cause" unless, as I assume is the case for both of us, our cause is getting closer to truth about the world :)
Got it…
Yup :)Elizabeth Liddle
May 28, 2011
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The broken GULO gene is not (direct) evidence of universal common ancestry, but it IS evidence for the common ancestry of a large subset of primates, including ourselves, i.e. that human beings descended from an ancestor whose descendents also included squirrel monkeys.
That is your opinion. However you cannot support that with genetic data linking to the transformations required. Do you really expect a broken gene to stay intact enough over thousands and thousands of generations all the while form-altering mutations are taking place?Joseph
May 28, 2011
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Joseph, yes I know my example was from the same, well not species (we are not the same primate species as squirrel monkeys!), but clade, and that was my (fairly simple) point. The broken GULO gene is not (direct) evidence of universal common ancestry, but it IS evidence for the common ancestry of a large subset of primates, including ourselves, i.e. that human beings descended from an ancestor whose descendents also included squirrel monkeys. And as I said, I'm not arguing that all broken genes are harmless (and an intact GULO gene would have saved thousands of sailors from scurvy). That wasn't my point at all - it was simply a point about common ancestry. As for Huntington's - yes, bearers of that gene might well "survive in the wild" long enough to rear young, so selective pressure against it would probably be weak. Conceivably it might even be positive (genes that result in early death of post-infant-rearing individuals my actually benefit their descendents by liberating precious resources). But that's not really the point - the point is not that the Vitamin C gene is evidence for positive selection - it isn't, if anything it's the opposite. What it is evidence for is common ancestry of a very large group of primates that includes ourselves.Elizabeth Liddle
May 28, 2011
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(And we can furthermore assume the individual in question lived in a fruit-rich environment, and so was able to flourish, despite the broken gene)
Sure we can make up any story we want to as long as it supports our cause. Got it...Joseph
May 28, 2011
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I don’t see how “common design” explains it – why would a designer disable a useful gene in a particular subset of species?
Not required. 1- Perhaps it was never a useful gene in all organisms- meaning it could have some other function 2- It was useful but then became disabled in several populations- mutational hot spots exist and a mutation via a common mechanism similarly disabled the working genes. Only populations that could supplement their diet (epigenetics) survived.Joseph
May 28, 2011
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Do you really expect a broken gene to stay intact enough over thousands and thousands of generations all the while form-altering mutations are taking place? Ya see your example is from the SAME species- ie LIMITED common descent. Do you think people with Huntington’s chorea would survive in the wild?Joseph
May 28, 2011
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Well, common descent explains it,because, just as a broken gene in a Dutch South African settler means that his (I think it was a man) descendants inherited the allele for Huntington's chorea, and that all people with Huntington's can trace their ancestry to that individual, it seems likely that all the individuals with a broken GULO gene can trace their ancestry to a common individual. And as those individuals include all members of the Haplorrhini ("dry-nosed") primates,to which we belong, it seems likely, does it not,that we haplorrhini can trace our ancestry back to a common ancestor in whom the first GULO gene was broken? (And we can furthermore assume the individual in question lived in a fruit-rich environment, and so was able to flourish, despite the broken gene). I don't see how "common design" explains it - why would a designer disable a useful gene in a particular subset of species?Elizabeth Liddle
May 28, 2011
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How does common descent expalain it? It just does? Do you really expect a broken gene to stay intact enough over thousands and thousands of generations all the while form-altering mutations are taking place? Common design explains it. There that is all I have to say because apparently that is all that is required.Joseph
May 28, 2011
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OK, thanks - so presumably you are suggesting that primates do not share a common ancestor, yes? That they were all created at some time, in some manner, with unbroken Vitamin C genes? And that they broke at some subsequent time? So how do you explain what would seem to be the odd coincidence of a subset of primates (including ourselves) having a broken version of that same gene? Why should exactly the same gene break in the same way in different lineages? On the other hand if primates have a common ancestor, and in one lineage, the GULO gene was broken, so that all descendents from that lineages inherited the same breakage, we have a neat explanation, even within Sanford's framework. The broken GULO gene is certainly not evidence in itself for evolutionary theory, but it is a powerful argument for common ancestry, is it not? Otherwise, how do you explain the distribution of the breakage across primate species?Elizabeth Liddle
May 28, 2011
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Elizabeth asks; 'if common descent is false, how do you account for the Vitamin C pseudo gene?' If it is truly a broken gene, which I really don't have complete knowledge of, It is explained by Genetic Entropy, which happens to be the true principle governing all 'beneficial' biological adaptations; Is Antibiotic Resistance evidence for evolution? - 'The Fitness Test' - video http://www.metacafe.com/watch/3995248 The following study surveys four decades of experimental work, and solidly backs up the preceding conclusion that there has never been an observed violation of genetic entropy: “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain - Michael Behe - December 2010 Excerpt: In its most recent issue The Quarterly Review of Biology has published a review by myself of laboratory evolution experiments of microbes going back four decades.,,, The gist of the paper is that so far the overwhelming number of adaptive (that is, helpful) mutations seen in laboratory evolution experiments are either loss or modification of function. Of course we had already known that the great majority of mutations that have a visible effect on an organism are deleterious. Now, surprisingly, it seems that even the great majority of helpful mutations degrade the genome to a greater or lesser extent.,,, I dub it “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain.(that is a net 'fitness gain' within a 'stressed' environment i.e. remove the stress from the environment and the parent strain is always more 'fit') http://behe.uncommondescent.com/2010/12/the-first-rule-of-adaptive-evolution/ Michael Behe talks about the preceding paper on this podcast: Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time - December 2010 http://intelligentdesign.podomatic.com/player/web/2010-12-23T11_53_46-08_00 Genetic Entropy, outlined by John Sanford in his book Genetic Entropy & the Mystery of the Genome, is when 'slightly detrimental' mutations, which are far below the power of natural selection to remove from a genome, slowly build up in a species/kind over long periods of time and lead to Genetic Meltdown. Evolution Vs Genetic Entropy - Andy McIntosh - video http://www.metacafe.com/watch/4028086bornagain77
May 28, 2011
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But what is the alternative explanation? Sure, evolutionary theory depends on more than "breaking things", but the question was just about common descent - if common descent is false, how do you account for the Vitamin C pseudo gene? I'm not saying you can't, but that that is the question :) Common descent explains it beautifully.Elizabeth Liddle
May 28, 2011
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Whoa nellie- don't ya think that common descent requires more than breaking things? IOW just how does universal common descet explain it? It just does? Are you saying that an organism with a broken vitamin c gene is more viable than an organism with a functioning VC gene? Can you demonstrate such a thing?Joseph
May 28, 2011
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Whoa, Nellie. What is the alternative explanation for the presence of the vitamin C pseudo-gene if not common descent?mike1962
May 27, 2011
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At least he's reading the book.paragwinn
May 27, 2011
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O/T: Darwin, Thomists, and secondary causalityMung
May 27, 2011
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Larry Moran is very easy to explain. If he's wrong (which he is) he has squandered his life and career on a lie, and he knows it. It's just that simple.GilDodgen
May 27, 2011
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This is classic Dr. Hunter: "Evolution and common descent have failed to explain how the original vitamin C gene could have arisen. In fact they fail to explain how any protein could have arisen. They have also failed to explain how all of biology could have arisen. This is not a good start." LOL,,, Definitely not a good start Dr. Hunter,, Not a good start at all! ==================== B. Reith Knockin On My Door - music video http://www.youtube.com/watch?v=_C4VzCpA19Ybornagain77
May 27, 2011
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No prediction, no retrodiction, and no falsification. Evolution and common descent do not prediction the vitamin C pseudogene, and they are not harmed if there was no such thing. This in addition to the fact that evolution and common descent do not explain how the original gene could have arisen in the first place. Moran’s assertion that the vitamin C pseudogene is powerful evidence for his unlikely idea appears to be just that, an empty assertion.
It do appear that way. Funny that Moran would be discussing this already. I wonder what he's goingto do when he gets to the Appendix in Wells' book (Appendix: The Vitamin C Pseudogene). My guess, he'll disregard everything Wells writes about it in the Appendix, claiming he's already dealt with the topic.Mung
May 27, 2011
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